The nucleus accumbens mediates a range of psychomotor behaviors through interactions with prefrontal cortex, mediodorsal thalamus, hippocampus and amygdala. Anatomical, physiological and pharmacological evidence ties accumbal function to a number of neuropsychiatric disorders, including schizophrenia. Several conceptual models have been proposed in which the accumbens gates recurrent flow to prefrontal cortex -however, the development of a more detailed, cellular-level model is required to explore the mechanisms by which such gating occurs. The complex biophysical characteristics of the medium spiny neurons, the principal cells of the accumbens, together with the changes in network dynamics induced by LTP and LTD of the extrinsic inputs, require cellular-level computational analysis. We will construct a biophysical-level model of the accumbens, together with sufficiently detailed models of prefrontal cortex and hippocampus, to investigate the role of the accumbens in gating of spatiotemporal spike input patterns. We will focus on the effects of dopaminergic modulation of network function, with D1, D2 and D3 receptor pathways modeled at the biophysical level. Our hypothesis, supported by recent experimental and theoretical studies, is that dopamine selectively amplifies network states based on goal-related salience. Large-scale network simulations will be directed at understanding the mechanisms of learning and selective gating of cognitive sequences, and of the role of nucleus accumbens in prepulse inhibition.